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GI- Week 2 > Fitzakerly: Anti-ulcer Drugs > Flashcards

Fitzakerly: Anti-ulcer Drugs Flashcards

1
Q

What diseases are treated w/ anti-ulcer drugs?

A
  1. Peptic acid disease (H. Pylori, NSAIDS)
  2. GERD and NER
  3. Hypersecretory States (hyperacidity, dyspepsia, stress ulcers, gastrinoma, systemic mastocytoses)
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2
Q

What are the objectives for treating PUD, hypersecretory diseases and GERD?

A
  1. Heal the lesion
  2. Stop the pain
  3. remove possibility of recurrence
  4. avoid complications
  5. eliminate maintenance doses
  6. prevent development of resistance
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3
Q

What are the treatment strategies?

A
  1. eliminate the cause (h. pyolori)
  2. Reduce pain by decreasing H secretion
  3. Eliminate NSAIDs
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4
Q

What are hte most effective drugs for preventing and treating peptic ulcer disease? Why?

A

Antimicrobials because they ERADICATE H. pylori

Amoxicillin
clarithromycin
metronidazole
rifabutin
tetracycline
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5
Q

What is the penicillin of choice for h. pylori? Why?

A

Amoxicillin

More acid stable

More than twice the blood levels are achieved w/ the same oral dose

Affective against gram -

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6
Q

What is the MOA and toxicity of Amoxicillin?

A

CIDAL
cell wall inhibitors

hypersensitivity

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7
Q

What is the macrolide antibiotic of choice for h. pylori treatment?

A

Clarithromycin

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8
Q

Why is clarithromycin better than azithro or erythro?

A

lowest MIC50 and is more acid stable

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9
Q

How do you compare azithro, clarithro and erythro?

A

Azithro and clarithro are better than erythro b/c they can be given at lower doses and have less GI effects.

Clarithro is better than azithro b/c the MIC90 is .06 vs. .25

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10
Q

What is the MOA of macrolides? Toxicity?

A

Static
Protein synthesis inhibitor (50S RNA)

GI irritation
drug interactions

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11
Q

What else can be used to treat h. pylori infections? Co administration with what can significantly decrease the antibiotic efficacy d/t chelation.

A

Tetracyclines

Antacids

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12
Q

You should always give tetracycline w/ ______NOT ________.

A

Food

NOT antacids

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13
Q

What is the MOA and toxicity of tetracyclines?

A

Static
protein synthesis inhibitors (30S)

Gi irritation
photosensitivity
discoloration of teeth (not good for pregnant women or children)

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14
Q

What drug is a bacterialcidal and inhibits hte DNA dep RNA pol?

A

Rifabutin= rifamycin

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15
Q

What are the SE of rifamycin?

A

Hypersensitivity/fever
hepatotoxicity
cyp 450 inhibition
orange/red body fluids

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16
Q

Why don’t we often use metronidazole/tinidazole to treat h. pylori?

A

up to 65% of infections are resistant

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17
Q

What is the MOA and SE of metronidazole/tinidazole?

A

DNA damage?

SE: GI, CNS toxicity, disulfiram rxn, teratogenic

Inhibits cyp2C9 (can potentiate warfarin and reduce clearance of H2 blockers)

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18
Q

What is the MOA of Bismuth?

A
  1. Antimicrobial- disrupts the cell wal and prevents adhesion or inhibits urease
  2. protects surface (coats surface and stimulates secretion of mucus, PG and bicarb)
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19
Q

Bismuth is only active in ______not_______.

A

stomach not the lower GI

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20
Q

Whare are the SE of bismuth subsalicylate?

A

Subsalicylate causes most SE: vomiting, tinnitus, confusion, hyperthermia, resp. alkalosis> met. acidosis

Bismuth: black tongue/stool

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21
Q

What are the causes of antimicrobial treatment failure?

A
  1. resistance (metronidazole and clarithromyacin)

2. compliance (too many pills for too long)

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22
Q

What drugs are used to eradicate H. Pylori?

A
  1. Amoxicillin
  2. Clarithromycin
  3. Tetracycline
  4. Rifabutin
  5. Metronidazole/tinidazole
  6. Bismuth subsalicylate
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23
Q

What drugs promote mucosal defence?

A
  1. bismuth subsalicylate
  2. misoprostol
  3. simethicone
  4. sucralfate
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24
Q

What antacids reduce intragastric acidity?

A
  1. aluminum hydroxid
  2. Ca carbonate
  3. magnesium hydroxide
  4. sodium bicarbonate
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25
Q

What antimuscarinics reduce intragastric acidity?

A
  1. atropine

2. pirenzipine

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26
Q

What H1 blockers reduce intragastric acidity?

A
  1. Cimetidine
  2. famotidine
  3. Nizatidine
  4. Ranitidine
  5. roxatidine
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27
Q

What PPI reduce intragasric acidity?

A
  1. lansoprazole
  2. omeprazole and esomeprazole
  3. pantoprazole
  4. raberprazole
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28
Q

What drugs are RARELY used to treat ulcers b/c they slow gastric emptying and prolong exposure of the ulcer to acid?

A

Muscarinic receptor ANTAGONISTS
Atropine
pirenzipine

*also have a more severe SE htan H2 blockers

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29
Q

How does ACh trigger acid secretion?

A

ACh acts on M1 (ECL) and M3 (Parietal cell) leading to acid secretion

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30
Q

What type of receptors are muscarinic receptors?

A

M1 and M3>
G protein linked>
activate phospholipiase C and D>
increase in IP3

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31
Q

What is the MOA of atropine and pirenzipine?

A

compeptive inhibitors of ACh

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32
Q

Which muscarinic receptor antagonist is M1 selective?

A

pirenzipine

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33
Q

What are the SE of atropine and pirenzipine?

A 
ABCD'S
Anorexia
blurry vision
constipation/confusion
dry mouth
sedation/stasis of urine
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34
Q

What drugs are NOT used to tx ulcers?

A

Muscarinic receptor antagonists

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35
Q

Overdose of atropine will cause…

A

CNS: hallucinations/ confusion
tachycardia
hot, dry skin

36
Q

What drugs are H2 receptor antagonists?

A

CIMETIDINE
famotidine
nizatidine
ranitidine

37
Q

What do H2 receptor antagonists do?

A

Decrease ALL forms of gastric acid secretion (esp nocturnal)

38
Q

Why are H2 receptor antagonists OTC?

A

they ahve few SE except cimetidine and can be given orally

39
Q

What is the primary effect of H2RAs?

A

They are competitive antagonists of H2 and are highly selective (no H1 activity)

40
Q

What is the secondary effect of H2 receptor antagonists?

A

Decrease intracellular cAMP> basal and nocturnal secretion d/t other agents

41
Q

What is the t1/2 of H2RA?

A

Usually 1-4 hrs but they have extensive hepatic metabolism and are excreted renally

42
Q

Which H2RA is hte best tolerated?

A

Famotidine (highest potency + smallest dose)

43
Q

What are the SE of H2RA?

A

No SE when given ORALLY to HEALTHY pt

44
Q

Why is it bad to give a pt rapid IV infusion of H2RA?

A

bradycardia and hypotension

*there are H2 receptors in the heart so you have to give a slow infusion

45
Q

What drug drug interactions are seen with H2RA?

A
  1. decreased ethanol metabolism (esp in women)

2. Compete for tubular secretion w/ weak bases (metronidazole)

46
Q

High doses of Cimetidine can cause…

A
  1. decrease binding of DHT to androgen receptors
    decreased estrogen metabolism
    incerased prolactin–>

gynecomastia and impotence in men
galactorrhea in women

  1. inhibition of cyp450 (increases effectiveness of other drugs)
47
Q

Which drug has a therapeutic advanatage esomeprazole or omeprazole?

A

Esomeprazole is exclusively the S isomer (omeprazole is the racemic mixture) and is metabolized more slowly and reproducibly

48
Q

What are the most effective agents for reducing intragastric acidity b/c they IRREVERSIBLY block the final common pathway in acid secretion—the H/K ATPase in the parietal cell?

A 
PPI:
esomeprazole/omeprazole
lansoprazole
pantoprazole
rabeprazole
49
Q

What drugs are good for treating GERD and ZE syndrome?

A

PPI

50
Q

Why do PPIs need a coating?

A

they are prodrugs that become labile in acid and must pass through the stomach to be absorbed

51
Q

Where are PPIs absorbed/concentrated?

A

SI then circulate throughout the body>
concentrate in teh acidified compartments>
protonated>
active form

52
Q

What should you give a PPI?

A

give drug 1/2 hr before meal so the concentration is highest when the pumps are active

53
Q

What are the SE of PPIs?

A

No sig SE

Some pts may experience HA, diarrhea, nausea, rash

54
Q

What is the danger of stopping PPIs in a pt who has been using them for a long time?

A

rebound acid hypersecretion

55
Q

What concerns are associated w/ long term use of PPIs?

A
  1. Decreased B12, FE, Ca, Zinc absorption> hip fx
  2. increased respiratory and enteric infections (increased pH)
  3. ECL hyperplasia (hypergasrinemia)
    Normally a decreased gastric pH> increases SS release> and leads to a decrease in gastrin
56
Q

What is used to buffer stomach acid?

A 
Weak bases:
Aluminum hydroxide
Ca carbonate
Mg hydroxide
Na Bicarbonate
57
Q

What weak bases are systemically absorbed?

A

NaHCO3 the most

CaCO2 some

58
Q

What drugs have a fast rate of dissociation?

A

NaHCO2 and CaCO2

59
Q

What weak bases create gas and can cause belching?

A

CaCO2 and NaHCO3

60
Q

aluminum hydroxide

A

Efficient and low systemic absorption

CONSTIPATION (not effective when given alone)

Decreases PO4 absorption> increased Ca loss> osteomalacia

61
Q

magnesium hydroxide

A

Efficient and low systemic absorption (like Al

OSMOTIC DIARRHEA

Renal insufficiency> hypermagnesemia> CNS and cardiotoxicity

62
Q

Calcium carbonate

A

Rapid onset of action and long duration

Belching/gastric distention, rebound acid secretion

MILD SYSTEMIC ALKALOSIS

63
Q

Na Bicarbonate

A

Extremely RAPID onset of action

bleching, gastric distention, short duration of action

SEVERE METABOLIC ALKALOSIS
ALKALINIZES URINE

64
Q

What drug interactions are associated w/ weak bases?

A
  1. increase gastric pH (can increase or decrease absorption)
  2. binds drugs (decrease absorption)
  3. increases gastric emptying (decreased absorption)
  4. systemic absorption (alkalinize urine)
65
Q

What is simethicone?

A

antifoaming agent that decreases gas pain

*also affects absorption

66
Q

What is the difference between antacids, H2 blockers and PPIs?

A

Antacids: rapid onset, short duration, INTERMITTENT DYSPEPSIA (don’t prevent ulcer recurrence)

H2 blockers: rpaid onset, intm duration, some prevention

PPI: slow onset, ong duration, EXCELLENT prevention

67
Q

What is the drug of choice for ZE syndrome, GERD and ulcer treatment?

A

PPIs

68
Q

What is sucralfate?

A

Al (OH3) and sulphated sucrose (NOT an antacid)

69
Q

What is the MOA of sucralfate?

A

attaches to ulcer surface (acts like a band aid)

70
Q

Sucralfate is used to tx?

A

stress induced ulcers in the ICU

71
Q

What does sucralfate require and what should it not be taken with?

A

acidic environment to be converted to paste

interacts w/ PPI and H2 blocker

72
Q

What are the SE of sucralfate?

A

constipation

binds other drugs

73
Q

What does misoprostol do?

A

replaces prostaglandins

74
Q

What percent of ulcers are caused by NSAIDs?

A

5%

75
Q

Why does misoprostol owrk?

A

PGE is less involved w/ inlammation and misoprostol t1/2 is 30-40 min compared to acetaminophen and ibuprofen (2hrs)

76
Q

What are the pharmikokinetics of misoprostol?

A

rapid absorption and metabolism

excreted in urine

77
Q

What are the SE of misoprostol?

A

diarrhea, severe nausea, cramping, abdominal pain

78
Q

What drug can also be used as an aborficant b/c it stimulates uterine contractions?

A

MIsoprostol

79
Q

What is triple therapy?

A

PPI + )clarithryomyacin for 5 days followed by amoxicillin or tinidazole for 5 days)

80
Q

What is quadruple therapy?

A

PPI + tetracycline + metornidazole + bismuch subsalicylate for 14 days

81
Q

What is a last choice therapy for ulcers?

A

PPI+ amoxicillin + rifabutin + cipro for 10 days

82
Q

At a low pH will you get more gastric absorption of WA or WB?

A

More of WA

83
Q

At a high pH will you get more gastric absorption of WA or WB?

A

WB will increase (PPI, H2 blocker, antacid)

84
Q

At a low pH will you get more excretion of WA or WB?

A

MOre WB

85
Q

At a high pH will you get more excretion of WA or WB?

A

More WA (antacids)

GI- Week 2 (11 decks)

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